Agents for treating ulcer have long been studied, and a numerous kinds of products have been developed. Peptic ulcer is caused by a high acidity of acid in the stomach, accelerated excitation of autonomic nerve, interruption in blood circulation in the walls of the stomach, stress, etc. As the anti-ulcerating agents, there have been used a mucous membrane-protecting agent and an aggressive factor inhibitor for inhibiting the secretion of acid in the stomach, such as H2 blocker and proton pump inhibitor. As the modern anti-ulcerating agents, there have been known an H2 blocker containing decreased numbers of granules and a proton pump inhibitor that inhibits the formation of granular super-oxide (non-patent document 1). In recent years, further, attention has been given to the wound-healing action of zinc (Zn), and an agent for treating the ulcer has been developed by blending an organic material with zinc (Zn). For example, there have been developed a histamine H2 acceptor by utilizing such a feature that a complex of zinc (Zn) can be easily incorporated, as well as a cimetidine/zinc complex obtained by blending the cimetidine of an antagonist with zinc (patent document 1).
Most of these agents for treating the ulcer are organic materials which may affect the safety of the human bodies.
As the inorganic agent for treating the ulcer, there have been used synthetic particulate hydrotalcites which are gastric antacids (patent document 2 and patent document 3). It has been said that the synthetic particulate hydrotalcites are ideal medicinal gastric antacids.
The synthetic particulate hydrotalcite that is a gastric antacid is also effective as an agent for treating the ulcer, and its preparation method has been disclosed in U.S. patent specifications (patent document 4 and patent document 5). The particulate hydrotalcite is typically represented by a chemical formula Mg6Al2(OH)16CO3.4H2O. When used as the agent for treating the ulcer, however, the conventional particulate hydrotalcite must be internally used for extended periods of time often causing damage to the mucous membrane of the internal walls of the stomach.                [Non-patent document 1] Digestive Diseases and Sciences, Vol. 45, No. 9, pp. 1786-1791 (September, 2000)        [Patent document 1] JP-A-6-49035        [Patent document 2] JP-B-46-2280        [Patent document 3] JP-B-50-30039        [Patent document 4] U.S. Pat. No. 3,539,306        [Patent document 5] U.S. Pat. No. 3,650,704        